We wish to continue our studies of the induction of thymic T-cell lymphomas in mice exposed to ionizing radiation or to chemical leukemogens. Specifically, we plan to investigate: 1. the contribution of lymphostromal and lymphoepithelial multicellular complexes to the thymus microenvironment essential for murine T-cell lymphomagenesis. 2. the role of natural killer (NK) cells and other mechanisms of immune surveillance in lymphomagenesis. 3. the hypothesis that viral envelope antigens induce autostimulatory blastogenesis leading to tumor development. 4. the evolution of autonomy of such lymphomas as related to phenotypic markers and chromosome numbers. 5. the hypothesis that radiation or chemicals activate an oncogenic replication-defective "xenotropic-like" retroviral genome which then induces apparently virus-negative lymphomas. 6. the hypothesis that lymphomagenic, replication-competent retrovirus may later be generated when such lymphomas are infected by a sporadically expressed non-oncogenic ecotropic virus, leading to "rescue' of the replication-defective "xenotropic-like" oncogenic genome. 7. the "promoter insertion" hypothesis and other possible molecular mechanisms of murine retroviral lymphomagenesis.